Mini review on photosensitization by plants in grazing herbivores

Abstract

Photosensitization is severe dermatitis or oxidative/chemical changes in the epidermal tissues activated by the light-induced excitation of molecules within the tissue. It is a series of reactions mediated through light receptors and is more common when the plant-produced metabolites are heterocyclic/polyphenols in nature. The areas affected are exposed body parts and mostly non-pigmented areas with least ultraviolet protection. Similarly, cellular alteration also occurs in the affected animal's dermal tissues and body parts and grazing animals by the accumulation and activation of photodynamic molecules. Photo-oxidation can also occur within the plant due to the generation of reactive oxygen species causing damage and degradation in the form of free radicals and DNA. During the last few decades, many new tropical grass species have been introduced in the grazing lands which are genetically modified, and the animals grazing on them are facing various forms of toxicity including photosensitization. The plant's secondary metabolites/drugs may cause toxicity when bacteria, viral agents, fungi (Pithomyces chartarum), or neoplasia injures the liver and prevents the phylloerythrin excretion. All these may disturb the liver enzymes and blood profile causing a decrease in weight and production (wool and milk etc.) with severe dermal, digestive, and nervous problems. Recent advancements in OMICS (cellomics, ethomics, metabolomics, metabonomics, and glycomics) have enabled us to detect and identify the plants' secondary metabolites and changes in the animal's physiology and histopathology as a causative of photosensitivity. The review focuses on types of photosensitization, reasons, secondary metabolic compounds, chemistry, and environmental effect on plants.

The aetiology, prevalence and morbidity of outbreaks of photosensitisation in livestock: A review

“…Several reviews of the incidence and prevalence photosensitisation in livestock have been published [1,4,26–31]. However, these have either focused on summarisation of diagnostic criteria [1,8,27,31,32], emphasised particular aetiological agents or been restricted to certain geographical regions [3,4,26,28,33]. As such, although providing useful information to the clinician or epidemiologist, they are generally limited in their ability to determine outbreak patterns, the prevalence of the causative agents, their relationship to morbidity, and the mortality on a larger scale.…”

Hepatogenous photosensitization by Brachiaria spp. in sheep: first report in Mexico

“…Jaundice and ulcerative dermatitis around the eyelids, pinnae, and nares in the sheep at the time of presentation were clinically suggestive of hepatogenous photosensitization (13,21). The serum chemistry in affected animals revealed a significant elevation of GGT, GLDH, AST and bilirubin, results that further supported the presumptive diagnosis of (5,11).…”

“…Steroidal saponins, the active toxic substance in Brachiaria spp., cause liver damage which in many cases culminate in hepatic failure and hepatogenous photosensitization (4,9,11,13,23). Affected sheep develop facial edema, alopecia, and necrotizing ulcerative dermatitis (1,12,13,21).…”

“…Steroidal saponins, the active toxic substance in Brachiaria spp., cause liver damage which in many cases culminate in hepatic failure and hepatogenous photosensitization (4,9,11,13,23). Affected sheep develop facial edema, alopecia, and necrotizing ulcerative dermatitis (1,12,13,21). As with all forms of photodynamic dermatitis, the most severely affected areas of the body are those covered with thin and poorly pigmented skin such as eyelids, nostrils, and pinnae (4,9,13).…”

“…Affected sheep develop facial edema, alopecia, and necrotizing ulcerative dermatitis (1,12,13,21). As with all forms of photodynamic dermatitis, the most severely affected areas of the body are those covered with thin and poorly pigmented skin such as eyelids, nostrils, and pinnae (4,9,13). As the condition progresses, the ruminant becomes lethargic, develop jaundice, neurological signs, and finally dies (1,13,21).…”